Table 3.
Summary of animal studies on E-liquid or E-vapor.
| Study | Animal | Exposure Material | Exposure Condition | Major Findings |
|---|---|---|---|---|
| Lerner et al., 2015 | C57BL/6J mice (8 wks old) | Vapor generated from Blu E-cig (Classic tobacco flavor, 16 mg nicotine) | Mice received 5 h whole body exposures to approximately 200 mg/m3 TPM per day for 3 successive days. | E-vapor exposure increased pro-inflammatory cytokines MCP-1 and IL-6, and diminished lung glutathione levels. |
| Lim and Kim. 2014 | BALB/c mice (Female, 5 wks old) | E-liquid (Z-company, Korea) ( 16 mg/ml nicotine) | 100 μL of 50-time diluted E-liquid was intratracheally instilled to OVA-sensitized (OVA-S) mice two times a week for 10 weeks. | Long-term exposure increased infiltration of eosinophils into airways from blood, stimulated the production of cytokines, including IL-4, IL-5 and IL-13, and OVA-specific IgE production. This study suggests that E-vapor exposure can exacerbate allergy-induced asthma symptoms. |
| McGrath et al., 2015 | C57BL/6J mice (Neonatal) | Vapor generated from Johnson Creek E-liquid (no flavoring, 0 and 18 mg nicotine). | Neonatal mice were exposed to 1.8% nicotine PG or 0% nicotine PG once a day for days 1 and 2 of life then twice a day from days 3 to 9 of life in a whole body exposure system. | E-vapor exposure during the neonatal period reduced weight gain, increased systemic cotinine, reduced alveolar cell proliferation and impaired postnatal lung growth. |
| Sussan et al., 2015 | C57BL/6 (Male, 8 wks old) | Vapor generated from NJOY e-cig (menthol flavor and “traditional bold”, 18 mg nicotine) | Mice were exposed in a whole body exposure system for 1.5 h for a total of 6 2-s puffs (35 mL) per minute, twice per day for 2 wks. | E-vapor exposure increased chemokine/cytokine release (IL-6, IFN-γ, TNF-α, IL-17A, MCP-1, and MIP-2), leading to oxidative stress and macrophage-mediated inflammation. E-vapor exposure also impaired pulmonary bacterial clearance due in part to reduced alveolar macrophage phagocytosis. E-cig exposure also increased lung Influenza A viral titers and increased Influenza A-induced illness and mortality. |
Abbreviations used in Table: ATP (adenosine triphosphate), LDH (lactate dehydrogenase), SPLUNC1 (short palate, lung, and nasal epithelial clone 1), PG (propylene glycol), HRV (Human Rhinovirus), MCP-1 (monocyte chemoattractant protein-1, CCL2), MIP-2 (macrophage inflammatory protein-2)